| pubmed-article:18716662 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18716662 | lifeskim:mentions | umls-concept:C0004364 | lld:lifeskim |
| pubmed-article:18716662 | lifeskim:mentions | umls-concept:C0015127 | lld:lifeskim |
| pubmed-article:18716662 | lifeskim:mentions | umls-concept:C1314792 | lld:lifeskim |
| pubmed-article:18716662 | lifeskim:mentions | umls-concept:C0011155 | lld:lifeskim |
| pubmed-article:18716662 | lifeskim:mentions | umls-concept:C1421876 | lld:lifeskim |
| pubmed-article:18716662 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:18716662 | pubmed:dateCreated | 2008-8-21 | lld:pubmed |
| pubmed-article:18716662 | pubmed:abstractText | Activation-induced cytidine deaminase (AID) expressed by germinal center B cells is a central regulator of somatic hypermutation (SHM) and class switch recombination (CSR). Humans with AID mutations develop not only the autosomal recessive form of hyper-IgM syndrome (HIGM2) associated with B cell hyperplasia, but also autoimmune disorders by unknown mechanisms. We report here that AID-/- mice spontaneously develop tertiary lymphoid organs (TLOs) in non-lymphoid tissues including the stomach at around 6 months of age. At a later stage, AID-/- mice develop a severe gastritis characterized by loss of gastric glands and epithelial hyperplasia. The disease development was not attenuated even under germ-free (GF) conditions. Gastric autoantigen -specific serum IgM was elevated in AID-/- mice, and the serum levels correlated with the gastritis pathological score. Adoptive transfer experiments suggest that autoimmune CD4+ T cells mediate gastritis development as terminal effector cells. These results suggest that abnormal B-cell expansion due to AID deficiency can drive B-cell autoimmunity, and in turn promote TLO formation, which ultimately leads to the propagation of organ-specific autoimmune effector CD4+ T cells. Thus, AID plays an important role in the containment of autoimmune diseases by negative regulation of autoreactive B cells. | lld:pubmed |
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| pubmed-article:18716662 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18716662 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18716662 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18716662 | pubmed:issn | 1932-6203 | lld:pubmed |
| pubmed-article:18716662 | pubmed:author | pubmed-author:OhnoHiroshiH | lld:pubmed |
| pubmed-article:18716662 | pubmed:author | pubmed-author:HaseKojiK | lld:pubmed |
| pubmed-article:18716662 | pubmed:author | pubmed-author:ItohKikujiK | lld:pubmed |
| pubmed-article:18716662 | pubmed:author | pubmed-author:TakahashiDais... | lld:pubmed |
| pubmed-article:18716662 | pubmed:author | pubmed-author:EbisawaMasash... | lld:pubmed |
| pubmed-article:18716662 | pubmed:author | pubmed-author:KawanoSayakaS | lld:pubmed |
| pubmed-article:18716662 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18716662 | pubmed:volume | 3 | lld:pubmed |
| pubmed-article:18716662 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18716662 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18716662 | pubmed:pagination | e3033 | lld:pubmed |
| pubmed-article:18716662 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:18716662 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18716662 | pubmed:articleTitle | Activation-induced cytidine deaminase deficiency causes organ-specific autoimmune disease. | lld:pubmed |
| pubmed-article:18716662 | pubmed:affiliation | Research Center for Allergy and Immunology, RIKEN, Yokohama, Kanagawa, Japan. | lld:pubmed |
| pubmed-article:18716662 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18716662 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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